Abstract: Disclosed herein is a genetically modified rodent animal comprising a humanized Clec9a gene in its genome. Also disclosed herein are an isolated rodent tissue or cell including a rodent embryonic stem cell, a rodent embryo, a method of making the genetically modified rodent animal, and methods of using the genetically modified rodent animal.

Abstract: This disclosure relates to a genetically modified rodent and use thereof as a rodent model. More specifically, this disclosure relates to rodent (e.g., mouse or rat) comprising a loss of function mutation in an endogenous Crnn (cornulin) gene, and to use of such a rodent animal as a rodent model of skin inflammation disorders (e.g., psoriasis).

Abstract: This disclosure relates to genetically modified rodent animals and rodent models of human diseases. More specifically, this disclosure relates to genetically modified rodents whose genome comprises a humanized Il1rl2 gene (coding for the IL1rl2 subunit of the IL-36R protein) and human IL-36?, ? and ? ligand genes. The genetically modified rodents disclosed herein display enhanced skin and intestinal inflammation as a preclinical model of psoriasis and IBD, respectively, and serve as a rodent model of human DITRA disease.

Abstract: The present disclosure relates to IL27 receptor agonists with improved therapeutic profiles.

Abstract: Provided herein are antibodies and antigen-binding fragments that bind MSR1 and methods of use thereof. According to certain embodiments, the antibodies bind human MSR1 with high affinity. In certain embodiments, the antibodies bind MSR1 without blocking, or blocking less than 90%, of modified LDL binding to MSR1. In some embodiments, the antibodies bind cell surface expressed-MSR1 and are internalized. The antibodies of the invention may be fully human antibodies. The invention includes anti-MSR1 antibodies, or antigen-binding fragments thereof, conjugated to drugs or therapeutic compounds.

Abstract: This disclosure relates to genetically modified rodent animals and rodent models of human diseases. More specifically, this disclosure relates to genetically modified rodents whose genome comprises a humanized Il1rl2 gene (coding for the IL1rl2 subunit of the IL-36R protein) and human IL-36?, ? and ? ligand genes. The genetically modified rodents disclosed herein display enhanced skin and intestinal inflammation as a preclinical model of psoriasis and IBD, respectively, and serve as a rodent model of human DITRA disease.

Abstract: Provided herein are antibodies and antigen-binding fragments that bind MSR1 and methods of use thereof. According to certain embodiments, the antibodies bind human MSR1 with high affinity. In certain embodiments, the antibodies bind MSR1 without blocking, or blocking less than 90%, of modified LDL binding to MSR1. In some embodiments, the antibodies bind cell surface expressed-MSR1 and are internalized. The antibodies of the invention may be fully human antibodies. The invention includes anti-MSR1 antibodies, or antigen-binding fragments thereof, conjugated to drugs or therapeutic compounds.

Abstract: The present invention provides antibodies and antigen-binding fragments (e.g., human antibodies) that bind specifically to human Interleukin-36 receptor (IL36R). Methods for treating or preventing diseases mediated by IL36R (e.g., skin or colon inflammatory conditions such as palmo-plantar pustular psoriasis, palmoplantar pustulosis, generalized pustular psoriasis, ulcerative colitis or IBD) using the antibodies and fragments are also provided along with methods of making the antibodies and fragments.

Abstract: Provided herein are compounds or payloads, linker-payloads, antibody-drug conjugates, and compositions, and methods for the treatment of diseases and disorders associated with the liver X receptor, including bis-octahydrophenanthrene carboxamides and protein (e.g., antibody) drug conjugates thereof.

Abstract: The present invention provides antibodies and antigen-binding fragments (e.g., human antibodies) that bind specifically to human Interleukin-36 receptor (IL36R). Methods for treating or preventing diseases mediated by IL36R (e.g., skin or colon inflammatory conditions such as palmo-plantar pustular psoriasis, palmoplantar pustulosis, generalized pustular psoriasis, ulcerative colitis or IBD) using the antibodies and fragments are also provided along with methods of making the antibodies and fragments.

Abstract: The present disclosure provides methods of treating subjects having an interferon mediated disease, methods of identifying subjects having an increased risk of developing an interferon mediated disease, and methods of detecting human Adenylate Cyclase 7 (ADCY7) variant nucleic acid molecules and variant polypeptides.

Abstract: This disclosure relates to a genetically modified rodent and use thereof as a rodent model. More specifically, this disclosure relates to rodent (e.g., mouse or rat) comprising a loss of function mutation in an endogenous Crnn (cornulin) gene, and to use of such a rodent animal as a rodent model of skin inflammation disorders (e.g.

Abstract: This disclosure relates to genetically modified rodent animals and rodent models of human diseases. More specifically, this disclosure relates to genetically modified rodents whose genome comprises a humanized Il1rl2 gene (coding for the IL1rl2 subunit of the IL-36R protein) and human IL-36?, ? and ? ligand genes. The genetically modified rodents disclosed herein display enhanced skin and intestinal inflammation as a preclinical model of psoriasis and IBD, respectively, and serve as a rodent model of human DITRA disease.

Abstract: Provided herein are antibodies and antigen-binding fragments that bind MSR1 and methods of use thereof. According to certain embodiments, the antibodies bind human MSR1 with high affinity. In certain embodiments, the antibodies bind MSR1 without blocking, or blocking less than 90%, of modified LDL binding to MSR1. In some embodiments, the antibodies bind cell surface expressed-MSR1 and are internalized. The antibodies of the invention may be fully human antibodies. The invention includes anti-MSR1 antibodies, or antigen-binding fragments thereof, conjugated to drugs or therapeutic compounds.